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C100095200v1
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Papers In Press, published online ahead of print April 10, 2001
J. Biol. Chem, 10.1074/jbc.C100095200
Submitted on February 20, 2001
Revised on April 10, 2001
Accepted on April 9, 2001

Characterization of the methylation-sensitive promoter of the imprinted ZAC gene supports its role in transient neonatal diabetes mellitus

Annie Varrault, Benoit Bilanges, Deborah JG Mackay, Eugenia Basyuk, Barbara Ahr, Céline Fernandez, David O Robinson, Joël Bockaert, and Laurent Journot

UPR 9023, Centre National de la Recherche Scientifique (CNRS), Montpellier, Cedex 05 34094

Corresponding Author: journot{at}ccipe.montp.inserm.fr

ZAC is a recently isolated zinc finger protein which induces apoptosis and cell cycle arrest. The corresponding gene is maternally imprinted through an unknown mechanism and maps to 6q24-q25, within the minimal interval harbouring the gene responsible for TNDM and a tumor suppressor gene involved in breast cancer. Due to its functional properties, imprinting status and expression pattern in mammary cell lines and tumors, ZAC is the best candidate so far for both disease conditions. In the present work, we delineated ZAC genomic organization and mapped its transcriptional start site. Noteworthily, the ZAC promoter localized to the CpG island harbouring the methylation imprint associated with TNDM and methylation of this promoter silenced its activity. These data indicate that the methylation mark may have a direct effect on the silencing of the ZAC imprinted allele. Our findings further strengthen the hypothesis that ZAC is the gene responsible for TNDM and suggest a novel mechanism for ZAC inactivation in breast tumors.


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